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Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
Plasma cells. Long-lived plasma cells are terminally differentiated cells that function to secrete large amounts of immunoglobulins and can persist for years. Most plasma cells home to the bone marrow, and, to a lesser extent, in the spleen, and peripheral tissues. Specialized niches of the BM allow the long-term survival of plasma cells, and the cellular population of plasma cells is hypothesized to be maintained through the continuous, antigen-driven differentiation of memory B cells. Plasma cells typically display a phenotype of CD20−, CD38high, CD27high, CD138+, TACI+ and/or BCMA+, CD126+, CD319+, and CD78+.
The Immunoglobulin Variable-Region Gene Repertoire and Its Analysis
Published in Cliburn Chan, Michael G. Hudgens, Shein-Chung Chow, Quantitative Methods for HIV/AIDS Research, 2017
Thomas B. Kepler, Kaitlin Sawatzki
Circulating mature B-cell subsets can be grouped into naïve, long-lived, and short-lived plasma cell and memory B cells. In peripheral blood mononuclear cells, 5%–20% is comprised of B cells. Although new B cells are produced throughout one’s life, there are characteristic changes in the repertoire. The majority of peripheral B cells consistently express a naïve phenotype, but 0%–20% express a memory phenotype, increasing with age. Plasmablasts make up 0%–5% and remain steady with increasing age [37]. Long-lived plasma cells primarily reside in splenic and bone marrow survival niches that provide appropriate survival signals and only rarely circulate. Long-lived memory B cells also persist in these survival niches but are commonly found in circulation [38,39]. It is clear that even in a sequestered state, these cells are capable of constant antibody secretion [40,41]. Most impressively, long-lived antibody memory is capable of lasting a lifetime, up to 89 years in one subject over 100 years old [40].
Human Influenza Virus Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Judith M. Fontana, Daniel P. Eiras, Mirella Salvatore
Although immunity to influenza virus infection is primarily mediated by the production of antibodies that are specific to the viral HA and NA surface proteins, cell-mediated responses (CD4+ T cells and cytotoxic T lymphocytes [CTLs]) are also a crucial component of protection. CD4+ T cells are particularly important for promoting the antiviral B cell response, which includes antibody class switching, affinity maturation, and generation of long-lived plasma cells.124 On the other hand, CTLs, which peak around day 14 post-infection,113 have been shown to contribute to viral clearance in influenza virus-infected individuals by destroying infected host cells through perforin/granzyme activity or Fas-FasL-mediated apoptosis.125,126 Additionally, CTLs produce proinflammatory cytokines that promote the recruitment and activation of other immune cells, particularly dendritic cells.127 Since CD4+ T cells and CTLs specifically recognize epitopes that are highly conserved, such as those within the NP and M1 viral proteins,128,129 these cells have also been implicated in mediating heterosubtypic immunity.130
Emerging role of monoclonal antibodies in the treatment of IgA nephropathy
Published in Expert Opinion on Biological Therapy, 2023
Dita Maixnerova, Vladimir Tesar
B cells and plasma cells play a role in autoimmune diseases [41,42]. Long-lived plasma cells are able to produce antibodies for several years and play a principal role in protective immunity and autoimmunity [41,43]. Recent data suggested that Gd-IgA1 might be produced predominantly by primed plasma cells in the mucosa [28,44]. Significantly higher percentages of CD38+ plasma cells have been found in patients with IgAN than in healthy controls [45]. The activation and durable preservation of antibody and autoantibody producing plasma cells have been associated with the upregulation of toll-like receptor 9 (TLR9), higher serum levels of B cell activating factor (BAFF) and increased expression of APRIL in patients with IgAN [29,30]. Plasma cells are defined by an abundant cell surface expression of CD38 and a loss of CD20 [41,43]. Therefore, anti-CD20 antibody therapeutics, such as rituximab, may deplete B cells but are not able to exclude plasma cells or decrease serum levels of Gd-IgA1 or anti-Gd-IgA1 antibodies [41,42,46,47] (Figure 3). A randomized controlled trial assessing rituximab in IgAN did not ascertain clinical utility compared to standard treatment [47].
Memory B cells and long-lived plasma cells in AMR
Published in Renal Failure, 2022
Wenlong Yue, Jia Liu, Xiaohu Li, Luman Wang, Jinfeng Li
Plasma cells are differentiated from activated B cells. As the final B cells to be produced, plasma cells can be classified into short-lived plasma cells and long-lived plasma cells from GC [60]. Long-lived plasma cells produce high-affinity, class-switched antibodies, while memory B cells have broader antigen specificity. Therefore, when antigens enter the human body, long-lived plasma cells produce neutralizing antibodies against antigens in the first phase of immune response. In the second phase of immune response, memory B cells play important roles by rapidly producing antibodies with high affinity against various pathogens [50,55]. In terms of surface marker expression, CD38 and CD138 generally colocalize on the plasma cell surface [61]. Garimalla et al. [62] reported ASCs, including plasma cells and long-lived plasma cells, in peripheral blood 7 days after tetanus vaccination. These ASCs lacked CD20 expression. CD20 is specifically expressed in the late stage of B-cell development, and the failure to detect CD20 may be an indication of successful B- cell conversion into plasma cells [63,64]. After clinical transplantation, mature GC B cells and memory B cells can be eliminated from patients with AMR with drugs targeting CD20 (such as rituximab), but this treatment cannot effectively reduce the concentration of DSAs, which is consistent with the absence of CD20 molecules on the surface of plasma cells.
Newly diagnosed multiple myeloma: current treatment strategies, emerging therapeutic approaches and beyond
Published in Expert Review of Hematology, 2020
Mehmet H Kocoglu, Ashraf Z Badros
Although the long-lived plasma cells are terminally differentiated and do not appear to be in desperate need of a robust proliferative capacity (even in their malignant counterparts), nonetheless, they need another skill-set for survival. Plasma cells are tasked with constant manufacturing of antibodies that requires a highly active endoplasmic reticulum and robust cellular secretory machinery. This physiological stress brings along a need for tightly controlled regulatory mechanisms one of which involves the proteasome. This organelle comes into play when there is a folding problem with scaffold of higher-structures of the proteins that give rise to non- or poorly-functional proteins (including both transcription factors and antibodies). This cascade that is responsible for repair of the salvageable- or removal of the unsalvageable-proteins is named “unfolded protein response (UPR)” [20]. In addition to the protein end-products of plasma cells, the realization of plasma cell addiction to transcription factors involved in normal homeostasis such as the NF-kB and effect on plasma cell survival was realized early on and revolutionized the way we treat myeloma today. Unlike the shared core structure of IMiD generations, PI generations chemically display significant differences of which two are in common clinical use.